Cavallin-Ståhl E, Mercke C, Lundh B
Br J Haematol. 1976 Feb;32(2):167-75. doi: 10.1111/j.1365-2141.1976.tb00919.x.
Endogenous production of carbon monoxide (VCO), red cell survival and iron kinetics were studied in 15 subjects with Hodgkin's disease. The subjects were divided into two groups, namely: eight patients with anaemia (group A, haemoglobin (Hb) concentration less than 11.5 g/dl) and seven patients without anaemia (group B, Hb concentration greater than 11.5 g/dl). Red cell survival was not significantly different in the two groups being 91 +/- 40 days (mean +/- 1 SD) in group A and 111 +/- 54 days in group B. Relative VCO (mumol/mmol total body haem (TBH/d) was, however, significantly higher (0.01 greater than P greater than 0.001) in group A (20.7 +/- 4.7) compared to group B (12.0 +/- 3.8). When absolute VCO (mumol/d) was compared to the daily turnover of circulating red cell haemoglobin haem (Vhaem-c), the VCO/Vhaem-c quotient was 2.1 +/- 0.9 in group A and 1.2 +/- 0.3 in group B. Erythron turnover of iron (ET, mumol Fe/mmol TBH/d) was calculated through subtraction of the non-erythron turnover (NET) from the total plasma iron turnover (PIT). ET was significantly higher (0.05 greater than P greater than 0.01) in group A (39 +/- 21) than in group B (20 +/- 8). The conclusion drawn from the finding of significant increases in VCO and ET without and concomitant significant decrease in red cell survival in the anaemia group is that ineffective erythropoiesis, i.e. bone marrow haemolysis, seems to play an important role in the anaemia of Hodgkin's disease.
对15例霍奇金病患者的内源性一氧化碳生成(VCO)、红细胞生存期和铁动力学进行了研究。将这些患者分为两组,即:8例贫血患者(A组,血红蛋白(Hb)浓度低于11.5 g/dl)和7例无贫血患者(B组,Hb浓度高于11.5 g/dl)。两组的红细胞生存期无显著差异,A组为91±40天(平均值±1标准差),B组为111±54天。然而,A组(20.7±4.7)的相对VCO(μmol/mmol全身血红蛋白(TBH/d))显著高于B组(12.0±3.8)(0.01>P>0.001)。当将绝对VCO(μmol/d)与循环红细胞血红蛋白血红素的日周转率(Vhaem-c)进行比较时,A组的VCO/Vhaem-c商为2.1±0.9,B组为1.2±0.3。通过从总血浆铁周转率(PIT)中减去非红细胞周转率(NET)来计算铁的红细胞生成周转率(ET,μmol Fe/mmol TBH/d)。A组(39±21)的ET显著高于B组(20±8)(0.05>P>0.01)。从贫血组中VCO和ET显著增加而红细胞生存期无相应显著降低的发现得出的结论是,无效红细胞生成,即骨髓溶血,似乎在霍奇金病贫血中起重要作用。